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  • 1
    Online Resource
    Online Resource
    Cervical cord compression from plexiform neurofibromas in neurofibromatosis 1
    BMJ ; 2007
    In:  Journal of Neurology, Neurosurgery & Psychiatry Vol. 78, No. 12 ( 2007-12-01), p. 1404-1406
    Details
    In: Journal of Neurology, Neurosurgery & Psychiatry, BMJ, Vol. 78, No. 12 ( 2007-12-01), p. 1404-1406
    Type of Medium: Online Resource
    ISSN: 0022-3050
    URL: Article
    DOI: 10.1136/jnnp.2007.121509
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2007
    detail.hit.zdb_id: 1480429-3
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  • 2
    Online Resource
    Online Resource
    Microwave photoconductivity decay characterization of high-purity 4H-SiC substrates
    AIP Publishing ; 2007
    In:  Journal of Applied Physics Vol. 102, No. 1 ( 2007-07-01)
    Details
    In: Journal of Applied Physics, AIP Publishing, Vol. 102, No. 1 ( 2007-07-01)
    Abstract: A microwave photoconductivity decay (MPCD) technique, which probes conductivity change in wafers in response to either an above-band-gap or below-band-gap laser pulse, has been used to characterize recombination lifetime in high-purity 4H-SiC substrates produced with three different anneal processes. The above-band-gap (266nm) decay times vary from ∼10ns to tens of microseconds in the 4H-SiC substrates depending on the wafer growth parameters. Wafers produced using the three processes A (as-grown), B (annealed at 2000°C), and C (annealed at 2600°C) have decay times of 10–20ns, 50–500ns, and tens of microseconds, respectively. The differences in decay times are attributed to low, medium, and high densities of recombination centers in process C, B, and A wafers, respectively. The MPCD results correlate with other characterization results such as deep level transient spectroscopy, which also showed that the 2600°C anneal process significantly reduces defect densities, resulting in the enhanced recombination lifetimes. Modeling and one-dimensional simulations indicate a trapping center closer to the conduction band results in a longer MPCD decay transient, but such a trapping based model for the enhanced lifetimes is not compatible with the wide range of experimental characterization results described in this work, which indicate an annealing out of recombination centers at 2600°C.
    Type of Medium: Online Resource
    ISSN: 0021-8979 , 1089-7550
    URL: Article
    DOI: 10.1063/1.2751086
    Language: English
    Publisher: AIP Publishing
    Publication Date: 2007
    detail.hit.zdb_id: 220641-9
    detail.hit.zdb_id: 3112-4
    detail.hit.zdb_id: 1476463-5
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  • 3
    Online Resource
    Online Resource
    Distinct Genetic Signatures among Pilocytic Astrocytomas Relate to Their Brain Region Origin
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 3 ( 2007-02-01), p. 890-900
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 3 ( 2007-02-01), p. 890-900
    Abstract: Pilocytic astrocytomas (PAs) are the most common glioma in children. Whereas many PAs are slow-growing or clinically indolent, others exhibit more aggressive features with tumor recurrence and death. To identify genetic signatures that might predict PA clinical behavior, we did gene expression profiling on 41 primary PAs arising sporadically and in patients with neurofibromatosis type 1 (NF1). Whereas no expression signature was found that could discriminate clinically aggressive or recurrent tumors from more indolent cases, PAs arising in patients with NF1 did exhibit a unique gene expression pattern. In addition, we identified a gene expression signature that stratified PAs by location (supratentorial versus infratentorial). Lastly, we also identified a gene expression pattern common to PAs and normal mouse astrocytes and neural stem cells from these distinct brain regions as well as a gene expression pattern shared between PAs and another human glial tumor (ependymoma) arising supratentorially compared with those originating in the posterior fossa. These results suggest that glial tumors share an intrinsic, lineage-specific molecular signature that reflects the brain region in which their nonmalignant predecessors originated. [Cancer Res 2007;67(3):890–900]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-0973
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    Nucleophosmin Mediates Mammalian Target of Rapamycin–Dependent Actin Cytoskeleton Dynamics and Proliferation in Neurofibromin-Deficient Astrocytes
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 10 ( 2007-05-15), p. 4790-4799
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 10 ( 2007-05-15), p. 4790-4799
    Abstract: Neurofibromatosis type 1 (NF1) is a common autosomal dominant tumor predisposition syndrome in which affected individuals develop astrocytic brain tumors (gliomas). To determine how the NF1 gene product (neurofibromin) regulates astrocyte growth and motility relevant to glioma formation, we have used Nf1-deficient primary murine astrocytes. Nf1−/− astrocytes exhibit increased protein translation and cell proliferation, which are mediated by Ras-dependent hyperactivation of the mammalian target of rapamycin (mTOR) protein, a serine/threonine protein kinase that regulates ribosomal biogenesis, protein translation, actin cytoskeleton dynamics, and cell proliferation. In this study, we show that Nf1-deficient astrocytes have fewer actin stress fibers and exhibit increased cell motility compared with wild-type astrocytes, which are rescued by pharmacologic and genetic mTOR inhibition. We further show that mTOR-dependent regulation of actin stress fiber formation, motility, and proliferation requires rapamycin-sensitive activation of the Rac1 GTPase but not elongation factor 4E-binding protein 1/S6 kinase. Nf1−/− astrocytes also exhibit increased protein translation and ribosomal biogenesis through increased expression of the nucleophosmin (NPM) nuclear-cytoplasmic shuttling protein. We found that NPM expression in Nf1−/− astrocytes was blocked by rapamycin in vitro and in vivo and that expression of a dominant-negative NPM mutant protein in Nf1−/− astrocytes rescued actin stress fiber formation and restored cell motility and proliferation to wild-type levels. Together, these data show that neurofibromin regulates actin cytoskeleton dynamics and cell proliferation through a mTOR/Rac1-dependent signaling pathway and identify NPM as a critical mTOR effector mediating these biological properties in Nf1-deficient astrocytes. [Cancer Res 2007;67(10):4790–9]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-4470
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
    Online Resource
    Online Resource
    TSC1 Sets the Rate of Ribosome Export and Protein Synthesis through Nucleophosmin Translation
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 4 ( 2007-02-15), p. 1609-1617
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 4 ( 2007-02-15), p. 1609-1617
    Abstract: Nucleophosmin (B23) is a nucleolar phosphoprotein that has been implicated in numerous cellular processes. In particular, nucleophosmin interacts with nucleolar components of newly synthesized ribosomes to promote ribosome nuclear export. Nucleophosmin is a classic mitogen-induced protein, with changes in its expression correlating with growth factor stimulation. In this study, we examined the underlying mechanism of nucleophosmin induction and showed that hyperproliferative signals emanating from oncogenic H-RasV12 cause tremendous increases in nucleophosmin protein expression. Nucleophosmin protein accumulation was dependent on mammalian target of rapamycin (mTOR) activation, as rapamycin completely prevented nucleophosmin induction. Consistent with this finding, genetic ablation of Tsc1, a major upstream inhibitor of mTOR, resulted in nucleophosmin protein induction through increased translation of existing nucleophosmin mRNAs. Increases in nucleophosmin protein accumulation were suppressed by reintroduction of TSC1. Induction of nucleophosmin through Tsc1 loss resulted in a greater pool of actively translating ribosomes in the cytoplasm, higher overall rates of protein synthesis, and increased cell proliferation, all of which were dependent on efficient nucleophosmin nuclear export. Nucleophosmin protein accumulation in the absence of Tsc1 promoted the nuclear export of maturing ribosome subunits, providing a mechanistic link between TSC1/mTOR signaling, nucleophosmin-mediated nuclear export of ribosome subunits, protein synthesis levels, and cell growth. [Cancer Res 2007;67(4):1609–17]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-2875
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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